Dermatology and Otology Update

Transcription

1 Dermatology and Otology Update by Rodney Rosychuk, DVM, DACVIM June 11, 2008 Sponsored by:

2 A DERMATOLOGY AND OTOLOGY UPDATE Rod A.W. Rosychuk DVM, DACVIM Page Canine atopy 2 Feline atopy 8 Golden Retriever Ichthyosis 11 Idiopathic Lymphocytic/Plasmacytic Pododermatitis 11 Feline Idiopathic Ulcerative Dermatitis of the Shoulder Area 12 Herpesvirus I Associated Dermatitis 12 Idiopathic Facial Dermatitis of Persian and Himalayan Cats 12 Canine and Feline Otology Video Otoscopy what it can do for you 14 Canine allergic otitis externa 15 Pseudomonas Otitis 22 Primary Secretory Otitis Media Cavalier King Charles Spaniel 27 Feline Otitis Externa 27 Feline Otitis externa due to Atopy 27 Feline Otitis Externa Due to Food Sensitivity 30 Feline Ceruminous Cysts / Ceruminous Cystomatosis 30 Feline Aural Polyps 31 Canine Bacterial Pyoderma 32 Canine Recurrent Bacterial Pyoderma 34 Conformational Pododermatitis Interdigital lesions 37 Comedones/Follicular Cysts Interdigital lesions 38 Canine Resistant Bacterial Infections 38 Acute Pseudomonal Pyoderma Syndrome 39 Canine Demodex 39 Feline Demodex 41 Diseases of the Planum Nasale 42 Discoid Lupus Erythematosus 42 Proliferative Arteritis 43 Hereditary Nasal Parakeratosis 43 Xeromycteria (Parasympathetic nose) 43 Canine Alopecia Alopecia X (Hair Cycle Arrest) 44 Recurrent Flank Alopecia 46 Color Dilution Alopecia 46 Canine Pattern Baldness 46 Post Clipping Alopecia 46 Sebaceous Adenitis 47 1

3 A DERMATOLOGY AND OTOLOGY UPDATE Rod A.W. Rosychuk DVM, DACVIM Colorado State University CANINE AND FELINE ATOPY: AN UPDATE CANINE ATOPY Important Points Regarding the Pathogenesis of Canine Atopy 1. Transcutaneous absorption of allergens is likely the major route for the initiation and perpetuation of the allergic response. Significance: frequent bathing helps to remove allergen from the surface of the skin. There is role for inhalation of these allergens, and even ingestion of allergens. The clinical signs associated with these routes of exposure appear to be less severe (i.e. transcutaneous > inhalation> ingestion). 2. It has been shown that the epidermal lipid barrier is disrupted in nonlesional atopic skin which may facilitate antigen uptake. It may also facilitate trans-epidermal water loss. Dry skin potentiates pruritus. 3. Although many of the skin changes associated with atopic dermatitis are related to self trauma, atopy can induce a primary skin eruption (erythema, maculo/papular eruption). 4. Allergic to: pollens of weeds, trees, grasses, house dust mites, molds, feathers, animal danders (cat, horse, cow, human), insects, storage mites (Tyrophagus putrescentiae, Leipidoglyphus destructor, Acarus siro), Malassezia. 5. Atopics in general are more prone to the development of bacterial colonization and infection of the skin with Staphylococcus intermedius. These infections are variably pruritic (may contribute very significantly to the pruritus/inflammation noted). Atopics may develop hypersensitivity reactions to Staphylococci and their by-products. Staphylococci may produce endotoxins that serve as superantigens which may actually perpetuate the allergic response. Reasons for predisposition to infection: Staphylococci stick more readily to the skin of atopic dogs when compared to normal dogss; seborrheic changes and self-trauma may produce a micro-environment more conducive to bacterial colonization. 6. Atopics are more prone to secondary colonization and infection with Malassezia pachydermatis. Malassezia may contribute significantly to pruritus. Individuals may develop hypersensitivities to Malassezia and its by products. Significance: relatively small numbers of Malassezia may contribute significantly to the development of inflammation and pruritus. 7. Genetic predisposition to the development of atopy has been well supported. In one recent study looking at atopic Labrador and Golden retrievers, breeding 2 atopic partents resulted in 65% of offspring being affected; breeding 1 atopic parent 21 57% affected; 2 non-atopics 11% affected. Diagnosis: Atopy remains a diagnosis predominantly made by history (e.g. seasonal pruritus), physical examination (e.g. distribution of pruritus and dermatitis facial, lip folds, ears, ventral cervical, feet, anterior elbows, axiallae, flanks, perianal, perivulvar, dorsum of back) and rule out. Major differential diagnoses include flea allergy dermatitis, food sensitivity, pruritic superficial bacterial pyoderma, Malassezia dermatitis, allergic contact dermatitis and generalized pruritic skin disease associated with intestinal parasite hypersensitivity in the young dog. Peripheral eosinophilia (CBC) and eosinophilic infiltrates in skin biopsies are uncommon. Inflammatory changes on skin biopsies are often non specific and most commonly are a perivascular accumulation of lymphocytes and macrophages. 2

4 Important Points Regarding the Management of Canine Atopy The recognition and management of secondary bacterial and Malassezia infections is mandatory! These secondary infections may contribute very significantly to pruritus. Similarily, the control of concurrent flea infestation/flea bite hypersensitivity is also mandatory in atopic patients. It has been shown that atopic individuals are more prone to the development of flea bite hypersensitivity! Topical Atopy Therapies 1. Shampoos and Conditioners: Shampoos containing oatmeal or oatmeal and pramoxine (a local anesthetic) may give a few hours of antipruritic activity. These shampoos are usually followed up with anti-pruritic conditioners to both treat and prevent the development of dry skin which may be a product of either the disease (atopy) or repeated bathing. The author prefers leave on conditioners for this purpose. These leave on conditioners are more likely to provide longer lasting anti-pruritic effects because they are not rinsed off after application. They include: oatmeal (ResiSoothe, Virbac), or 1% hydrocortisone (ResiCort, Virbac). The hydrocortisone product appears to have superior anti-pruritic activity. However, for cost/benefit purposes, the author most frequently uses the ResiSoothe product. In that many of our atopic patients are prone to recurrent bacterial and Malassezia infections, it is very common for us to use a germicidal shampoo (e.g. Malaseb with chlorhexidine and miconazole; DVM pharmaceuticals or Douxo, Chlorhexidine PS; Sogeval) on a maintenance basis. This is then followed by the use of an antipruritic conditioner (e.g. ResiSoothe, Virbac). The residual conditioner can also be used by itself (without shampoo) between baths to help reduce pruritus. Newer additions to our armamentarium of shampoos and conditioners are those that contain phytosphingosines (anti-microbial, anti-inflammatory, pro-ceramide; help to normalize barrier function). In addition to phytosphingosines, they contain Hinokitiol (red cedar extract; anti-inflammatory, antimicrobial, antifungal) and raspberry seed oil (antioxidant, normalizes stratum corneum). These products include Douxo Calm Shampoo (initially used every 3-7 days), Douxo Calm Micro-emulsion Spray (initially used every 3 days, then every 3-7 days long term for maintenance and Douxo Calm Gel for localized lesions (daily for 8 days). 2. Topical glucocorticoids a. 1% hydrocortisone products (e.g. CortiCalm by DVM, DermaCool-HC by Virbac or ResiCort by Virbac) are applied BID or TID initially. Therapy is usually used for 2-3 days to suppress flares of atopic dermatitis. Emphasis is placed on infrequent use to minimize local side effects of the glucocorticoid (hair loss, cutaneous atrophy, follicle plugging, and predisposition to infection). b..015% triamcinolone acetonide spray (Genesis Topical Spray; Virbac). For moderate to severe flares of atopic dermatitis, the spray is administered BID for one week, then once daily for one week, then once every other day for a week. Absorption is minimal if label dosages (number of pumps per treatment) are adhered to. In one study, polyuria was reported in 3 and polyphagia in 1 of 57 dogs treated for 3 weeks. There was no notation of the exacerbation of pyoderma in treated individuals but this should be closely monitored for. Long term use should be restricted to treating localized flares of atopic dermatitis spray or rub on affected areas once or twice daily for 1-3 days; no more than once every two weeks. This product has proven very beneficial for better controlling the more focal manifestation of atopic pruritus. It should be noted that too frequent application, over long 3

5 periods of time (e.g. once every other day for 8 12 months) may produce significant regional hair loss, cutaneous atrophy and predisposition to local infections. Sufficient glucocorticoid may be absorbed to contribute to the development of generalized iatrogenic hyperadrenocorticism (e.g. widespread hair loss, cutaneous atrophy). The product must be used with respect! 3. Tacrolimus (Protopic; Fugisawa; 0.1%) is an inhibitor of T-lymphocyte activation. It is noted to be times as potent as cyclosporine. Absorption from the skin is minimal. It is initially applied BID. This product may be beneficial for the more focal, at times refractory manifestations of atopy (e.g. pododermatitis or perianal pruritus). Its cost precludes use over large areas of the body. Tacrolimus appears to do a better job of reducing the inflammation associated with atopic dermatitis as compared to pruritus, but may work for both. This product appears to be superior to the less costly pimecrolimus (Elidel; Novartis), whose mode of activity is similar to that of tacrolimus. Glucocorticoids Prednisolone/prednisone starting at mg/kg given once daily; slowly tapered to the lowest every other day dose required to control signs; ideally < 0.25 mg/kg every other day. Alternatives to prednisone / prednisolone include metylprednisolone (associated with a reduced incidence of PU/PD; same dosages as prednisone) or Temaril-P (5 mg of trimeprazine, an antihistamine and 2 mg of prednisolone per tab; Pfizer). The Temaril-P product may allow for lesser dosages of glucocorticoid because of the antihistamine included. Prior to considering glucocorticoids for longer term maintenance, every effort should be given to provide glucocorticoid alternatives. When this is not possible, the author will usually try to maintain the patient on the lowest, once every other day dose of Temaril-P possible. Lower dosages of Temaril-P are often facilitated by using Temaril-P along with a full, recommended daily dose of another antihistamine such as chlorpheniramine, diphenhydramine, hydroxyzine, amitriptyline, or clemastine. With any long term, even low dose glucocorticoid therapy, it is important to monitor for signs of iatrogenic hyperadrenocorticism (dry coat / skin; mild hair loss; gradual weight gain; increased propensity to develop bacterial pyoderma; increased propensity to develop urinary tract infections). Fatty Acids Controversy continues to exist as to which fatty acid and which ratio of fatty acid (omega 6:3) to use in optimizing anti-inflammatory, anti-pruritic effects. Products rich in n-3 fatty acids (cold water fish oils and flaxseed) appear to be favored. Our impression is that benefit is directly proportional to dose. In a study completed at CSU, dogs treated with about 85 mg/kg of a combination of Eicosapentanoic acid (EPA) and docsahexanoic acid (DHA) (equivalent to about 1 Giant breed 3V Cap per 5 kg body weight which is about 3 times the recommended label dose), 40 50% improved by greater than 50%. Complete remission was obtained in 10 20%. This, however, is a very high dose of fatty acid. At present, we start our fatty acid therapy in the range of mg/kg/day EPA and DHA (combined). It is suggested that fatty acid containing products should be given at least a 12 week trial before they are critically evaluated. However, benefits may be noted within the first 2-3 weeks of therapy. Research by Iams has shown that a 5:1 to 10:1 ratio of omega-6 to omega-3 fatty acid in the overall diet may be ideal for management of inflammatory skin disease in the dog. Their restrictive diets (e.g. Eukanuba TM Response Formula fish and potato and their kangaroo and oat diet) contain this ratio of fatty acids. Our own uncontrolled studies evaluating the efficacy of the fish and potato diet in 47 atopic dogs showed a greater than 50% reduction in pruritus in 42% of dogs. 4

6 Antihistamines Antihistamines appear to benefit about 30% of our atopic patients. Both first generation H1 blockers (e.g. chlorpheniramine, diphenhydramine) and second generation products that fail to cross the blood brain barrier (e.g. loratidine) appear to have similar success rates. It is felt that one cannot predict which, if any antihistamine will be of help in a given individual. We generally have the owner try several different antihistamines, each for 2 weeks (3 or 4 weeks if the owner is not very observant). The owner notes which antihistamine is being used and what degree of benefit, if any, it may produce. The following are the antihistamines used most frequently in our practice. Where available, we recommend the cheapest generic products available. Those with an asterisk tend to be most effective/cost effective (unless otherwise marked): * Hydroxyzine HCl mg/kg BID or TID ; * Chlorpheniramine mg/kg BID to TID ; * Diphenhydramine mg/kg BID or TID; *Amitryptyline- 2.2 mg/kg BID; *Clemastine (Tavist or generic) -.05 mg/kg BID or for dogs under 10 kg 1/2 tab BID; kg, 1 tab BID, bigger, 1 1/2 tab BID; Cyproheptadine mg/kg TID; Doxepin HCl mg/kg BID. Which is the most effective? Some studies have suggested clemastine; another study suggested hydroxyzine and diphenhydramine. The author has had best results with hydroxyzine, followed by chlorpheniramine. H 1 blockers have antihistaminic, antichollinergic, sedative and local anesthetic effects. They must be used with caution, if at all, in the presence of liver disease, glaucoma, urinary retention, gastrointestinal atony and pregnancy. Other newer antihistamines include cetirizine ( 10 mg/day/animal < 25 kg and 10 mg BID > 25 kg), loratidine ( mg/kg/day) and astemazole (.25 mg/kg q24hr). It has been suggested that cetirizine may be the most effective of this group. Combinations of antihistamines may be of benefit when individual antihistamines themselves appear to have failed. Combinations are also considered for the initiation of therapy when individuals are more significantly pruritic (especially if glucocorticoids are not an option). The author has had most success with the combination of chlorpheniramine and hydroxyzine; second choice would be chlorpheniramine and amitriptyline. We have used virtually all antihistamines in combination and, at times have used as many as three antihistamines at the same time; all toerlated well. The antihistamines are used at full dosages. Pentoxifylline Pentoxifylline (a phosphodiesterase inhibitor; Trental or generic) has been noted to reduce the pruritus and erythema associated with atopy at a dosage of 10 mg/kg BID, although TID administration at dosages as high as mg/kg may be more beneficial. The author routinely starts therapy in the mg/kg BID range. The author has, in general, been disappointed with this drug as a monotherapy for atopy. It may help to reduce steroid dosages in patients on glucocorticoids, and may work synergistically with antihistamines. It is therefore usually used along with an antihistamine or glucocorticoid as part of a combination therapy. It is generally tried when other, more conventional therapies have failed. Cyclosporine Oral cyclosporine at a dose of 5 mg/kg/day has now been evaluated in at least 9 studies for its effectiveness in treating canine atopy. Preferential forms based on bioavailability and clinical efficacy are Atopica, Novartis and Neoral, Novartis. Although the results in these studies varied, approximately 75% of patients have been noted to significantly benefit from therapy. When compared to other interventions, cyclosporine was about as effective as oral glucocortiocids. The recommended trial period, based on response, was 4-6 weeks. Once > 50% improvement was noted, dosage frequency could be reduced to q 48 hrs in 40 60% of cases and q 72 hrs in about 20%. Successful control could be managed with lower daily doses (1/2 dose) in about 40% of patients and ¼ dose in about 40%. The major side effect encountered is gastrointestinal upset (vomition, diarrhea, flatulence, abdominal cramping with vomition being 5

7 most common). Cyclosporine had to be discontinued in approximately 5% of individuals because of these side effects. In this author s experience, the incidence of vomition may be minimized by gradually working up to the maintenance dose over several days (e.g. 5-7 days). In spite of the fact that the concurrent administration of food with cyclosporine does reduce bioavailability (reduced by approximately 20%), this does not usually affect clinical efficacy. For this reason, the author gives cyclosporine with a small amount of food, to further reduce the incidence of GI upsets. Once it is clear that the drug is well tolerated, it is given on an empty stomach (at least 2 hours before feeding). If vomition is noted, the drug should be stopped until this side effect has resolved and can be tried again. It is often tolerated the second time around. Metoclopramide, give minutes prior to cyclosporine administration may also used to minimize vomition ( mg/kg). It has been suggested that freezing the cyclosporine capsules prior to administration may also reduce this tendency to encounter vomition. Other uncommon to rare side effects reported in dogs include anorexia, gingival hyperplasia (usually resolves with discontinuation of cyclosporine; may be improved with azithromycin therapy while remaining on cyclosporine), papillomatosis (usually resolves with discontinuation of cyclosporine), bacteriuria, bacterial pyoderma, opportunist fungal infections, tremors, seizures, nephropathies, bone marrow suppression and a lymphoplasmacytic dermatosis. Although the trial period to assess effectiveness is 4-6 weeks, it may take 2-4 months to see the maximal benefit of the therapy (usually plateau s at 3 months). Once the maximal benefit has been noted, the dose is reduced to every other day, then every 3 rd day. If every other day dosing does not hold the problem, then return to daily dosing and once the problem is again quieted down, gradually reduce the once daily dose to the least amount required to control the problem. It is very interesting to note that a small number of patients may be able to have their oral cyclosporine eventually stopped, with a complete remission of disease (no recurrence; Olivry - 10% of cases; Radowiz 24%). In that cyclosporine is expensive, it has been used in conjunction with ketoconazole to increase the blood concentrations of the cyclosporine. We start with 2.5 mg/kg cyclosporine per day (gradually working up to this dosage) along with mg/kg ketoconazole once per day. A higher dose of ketoconazole (i.e. 10 mg/kg/day) may be associated with higher circulating cyclosporine concentrations and greater anti-pruritic benefits. The ketoconazole is given with a small amount of food. Cyclosporine is initially given with a small amount of food, then eventually tried without food (at least 2 hours before or after feeding). Metoclopramide, at a dosage of mg/kg, give about ½ hour prior to giving cyclosporine, has also been noted to enhance the absorption of cyclosporine by up to 30% in man and has been anecdotally suggested to do so in dogs. It has been suggested that the dosage of cyclosporine can be reduced by 1/3 to ½ in individuals pre-treated with metoclopramide. In general, blood trough levels of cyclosporine do not correlate well with clinical efficacy. However, they can be of value to if there is concern for cyclosporine toxicity (values higher than 500 ng/ml suggest the possibility of toxicity) or if there is a lack of clinical effect with a given dosage regimen. In the latter case, if the blood cyclosporine concentrations are very low (e.g. < 50 ng/ml), then consideration could be given to increasing the dose of cyclosporine. A blood sample (minimum of 0.5 ml whole blood, collected in purple-top tube; sample should not be centrifuged; may be frozen or kept cold in refrigerator until analysis; stable for 30 days at C (frozen) ) is taken just before the next dose of cyclosporine. When using a specific radioimmunoassay or HPLC, true concentrations of cyclosporine are measured. But, when using a TDx fluorescence polarization assay (monoclonal whole blood), multiply the feline concentrations by 0.5 to get the true concentration, and multiply the canine concentration by 0.6 to get the true concentration. 6

8 Hyposensitization Hyposensitization based on data generated by either intradermal testing or in vitro serologic testing produce very similar success rates. Hyposensitization, using aqueous preparations, is noted to benefit 60 70% of cases (good to excellent results). Over the long term, 50-70% of our patients on hyposensitization require additional medication (antihistamine, steroid and/or fatty acids) to control allergic signs during part or all of the year. The majority of our patients on maintenance hyposensitization get their shots every 1-2 weeks during the allergy season. For patients who derive only transient benefits from a given shot (2-3 days), we divide our solutions and give.5 cc twice weekly, or even smaller volumes up to three times a week (e.g. 0.2 cc three times weekly). It is also very important to monitor for increased pruritus following a given shot. Affected individuals may actually have their allergy signs significantly worsened if they react to the hyposensitization solution. If such is the case, we reduce the volume of solution to that which did not produce a reaction. Patients noted to have reactions to shots appear to have an overall better chance of deriving benefit from the shots, assuming the volume and frequency of solution are managed appropriately. Rush immunotherapy, which involves giving all the induction dosages in the hyposensitizing protocol in one day has been shown to produce a more rapid onset of benefit from hyposensitization and an overall higher success rate. The incidence of significant side effects from this protocol has been very low. Patients are pre-treated with an antihistamine at least 2 hours prior to beginning the protocol. Patients are then given their gradually increasing dosages of aqueous hyposensitization solution SubQ every half hour until the full maintenance dose of 1 cc of the maintenance solution (usually 20,000 PNU/ml) is reached. Once the Rush is completed, the patient is placed on the 1 cc per week maintenance dose of solution until the maximal benefit of the solutions is noted. If any significant reaction is noted to a given shot during the Rush protocol, (most common is increased pruritus), then the protocol is stopped at this time. The next lower dose that failed to cause this reaction is used as the once weekly maintenance dosage. At the end of a 12 month trial, assuming a lack of response, dosages are gradually reduced (e.g. 0.5 cc once weekly for one month, then 0.2 cc once weekly for one month) to see if low dose therapy may be of benefit. This is done instead of just stopping the solutions at the end of the 12 month trial. Low dose therapy may actually be of more benefit than routine dosages in some individuals. It is interesting to note that in one recent study (Power H et al,), 29% of patients who discontinued hyposensitization shots did so because the atopy went in to spontaneous remission. We quote a 10% - 15% chance individuals with be able to discontinue hyposensitization and their atopy will remain in remission. This is often not noticed until patients have been doing very well on hyposensitization for protracted periods of time (e.g. 2-3 years). 7

9 FELINE ATOPY In the older Veterinary literature, it has often been suggested that the incidence of atopy is similar to that of food sensitivity in the cat. However, in our clinic, for cats showing the clinical signs listed below, about 70% are noted to be atopic and 20% food sensitive, 10% a combination of both. This relative incidence of disease may have significant regional variation! Feline atopy is associated with a myriad of clinical signs. These may include: 1. Alopecia with or without dermatitis due to self trauma (may be a symmetric, self induced alopecia; higher prevalence areas tend to be the ventral abdomen, caudal thighs, dorsomedial forelimbs) 2. Pruritus directed at and restricted to the head and/or neck 3. Pruritic miliary dermatitis (lesions most commonly over the back, sides and head) 4. Eosinophilic plaques (pruritic) most commonly over the medial thighs and ventral abdomen, but may be found over any area of the body 5. Indolent ulcer upper lip or lips; may be the only manifestation of atopy in a given individual 6. Eosinophilic granuloma variable pruritus; lesions may be found anywhere over the body; higher incidence in chin area, caudal thighs (linear granuloma) and oral cavity (hard and soft palate). 7. It is possible to see any of the manifestations of the eosinophilic granuloma complex (eosinophilic plaques, indolent ulcer, eosinophilic granuloma) in the same cat. 8. Recurrent or persistent otitis externa; may be associated with other skin lesions or may be the only manifestation of atopy; although usually bilateral, may be predominatly bilateral. 9. Pruritic lesions may predominate in the chin and perioral region as diffuse erythema and the accumulation of dark exudates, giving the impression of feline acne; however, when clipped, classic comedo formation is not noted. However, if a patient does have feline acne, it would appear that atopic dermatitis in the chin area can worsen feline acne signs (i.e. increased comedones). 10. Secondary bacterial pyoderma occurs but is less common than in the dog. 11. Secondary Malassezia infections are noted, but are less common than in the dog. They tend to predominate in the facial (folds, lip margins, chin) and foot areas (interdigital; nail folds). 12. Rhinitis, conjunctivitis 13. Asthma with or without any of the cutaneous signs noted above (may be the only sign of atopy). It is also quite common to see subclinical respiratory signs (tracheal irritability; readily induced cough with compression of the trachea; rales on auscultation) in atopic cats. Diagnosis The finding of a peripheral eosinophilia and basophilia in a CBC is common in atopic cats. Biopsies from affected areas commonly show increased numbers of mast cells and eosionphils (suggesting a hypersensitivity disorder but not defining the type of hypersensitivity disorder). The above diagnostic aids are considered supportive. The diagnosis of atopy is largely based on history and rule out (e.g. especially rule out flea bite hypersensitivity, food sensitivity). 8

10 Therapy 1. The therapy of feline atopy should always include the documentation and treatment of secondary bacterial or Malassezia infections. These are best defined by cytologic examination. 2. Glucocorticids: Because glucocorticoids are well tolerated in the cat, they tend to be the cornerstone of therapy. However, as the disease becomes more chronic and severe, it is not uncommon to have the patient require higher dosages, more frequent dosage administrations or more potent glucocorticoids to maintain comfort. It has been shown that prednisolone is more bioavailable and has improved drug kinetics when compared to prednisone in cats and therefore prednisolone is the drug of choice in cats. Cats are often started on 1 2 mg/kg/day of prednisolone; goal for long term therapy would be < mg/kg every other day. Depo" steroids are acceptable for periodic administration (ideally keep frequency of administration to less than once every 6-8 weeks - methylprednisolone acetate or triamcinolone acetonide). For patients refractory to prednisolone consideration should be given to using the longer acting, more potent oral dexamethasone ( m/kg/day to start) or triamcinolone acetonide (0.5 1 mg/kg/day; maximum of 4 mg/cat/day to start). Emphasis should always be placed on reducing dosages of these longer acting, more potent steroids to the lowest dosage possible, given every 2 nd to 3 rd day. Ideally, once improvement has been noted on these more potent steroids, an attempt should be made to switch back over to prednisolone for longer term therapy. 3. Fatty acids such as 3V caps (DVM pharmaceuticals; omega 3) benefit approximately 20-30% of cases (some quote 30 50%). Many cats, however, refuse to eat the fatty acids. Trial period is 3 months. 4. Antihistamines: The antihistamines that have been of most benefit in our hands for treating feline atopy are chlorpheniramine (2-4 mg/cat q 12 hrs) or amitriptyline ( mg/cat q hrs). Amitriptyline may cause significant sedation, ataxia etc.; cats may salivate excessively when it is given. To minimize the chances of encountering sedation, the author starts at 2.5 mg total dose in the evening. If this is tolerated, 2.5mg is given in the AM and 2.5 mg in the PM. If this is tolerated, but is not beneficial to the pruritus, the dose is increased to 5 mg in the evening, 2.5 mg in the morning, then 5 mg BID if necessary. Problems with palatability can be circumvented by using amitriptyline powder mixed in fish/cod liver oil. Other antihistamines to be tried include clemastine fumarate ( mg/cat BID), ceterizine (.5 1 mg/kg or 5 mg/cat) or cyproheptadine (2 mg/cat BID; may cause polyphagia and behavioral effects). Each is tried for 3 weeks. 5. Hyposensitization: Hyposensitization has been reported to benefit anywhere from 45% to 75% of cases. Our success rate has been in the 60-70% range. Testing to determine allergens for inclusion in hyposensitization protocols may either be with intradermal testing or in vitro serology or both. Data from either type of testing appears to be associated with relatively similar success rates of hyposensitization. Protocols for hyposensitization using aqueous allegens are similar to those used for the dog. The author uses the same frequency of administration, but only 1/2 the volumes. Rush immunotherapy has been conducted successfully in cats but, until there has been more experience with this protocol, it should be used with great caution. 9

11 6. Cyclosporine: Oral cyclosporine has been noted to work well in the management of atopic dermatitis in the cat. Cats are generally treated with 5 10 mg/kg/day. The author s initial target dose is 5-7 mg/kg/day initially. This is worked up to over several (4-6) days; e.g. 10 mg q24 hr for 2 days, then 20 mg q24 hr for 2 days, then 25 mg daily thereafter. It is given with a small amount of food. Once it is clear that the cyclosporine is tolerated well (i.e. after 10 to 14 days therapy), it is given without food to enhance absorption (at least 2 hours before or after feeding). It is given with a small amount of food. Once it is clear that the cyclosporine is tolerated well, it is given without food to enhance absorption. If the cat will not tolerate the capsules, then the cyclosporine can be aspirated from the capsules and given per os, or mixed with food and given per os. Cyclosporin at this dosage appears to be tolerated reasonably well. However, gastrointestinal upsets (nausea, vomition, inappetence, anorhexia) are relatively common. If GI problems are encountered, the drug is stopped until the signs have abated and it is then re-instituted. We have seen apparently latent toxoplasmosis exacerbated while on this therapy (likely because of the immunosuppressive effect of cyclosporine) but this appears to be uncommon. Toxoplasmosis titers taken prior to the administration of cyclosporine are of questionable value. The lack of a titer may actually suggest that the individual is more susceptible to infection. Cats on cyclosporine should not be allowed to hunt (especially if they have a negative toxoplasmosis titer). See comments under Canine atopy for information regarding the measurement of trough cyclosporine concentrations. 7. Chlorambucil has also been of benefit (usually along with standard, antiinflammatory/antipruritic dosages of steroids, as noted above) in treating refractory atopy. The recommended dose is of chlorambucil is mg/kg q 24 hrs until 75% improvement in clinical signs, then this dose given every other day. Adverse effects to be monitored for include bone marrow suppression and hepatotoxicity (i.e. should be normal liver enzymology prior to treatment; recheck liver enzymes at 2-3 weeks and 4-6 weeks in to therapy; CBC and platelet count every three weeks while on daily therapy, gradually taper off during every other day therapy). 8. Megestrol acetate may be considered a "last ditch" alternative for treating feline atopy, in light of potential side effects ( polyphagia / weight gain, PU/PD, personality and behavioral changes, pyometra or stump pyometra, mammary hyperplasia, mammary neoplasia, diabetes mellitus and adrenal suppression). Remission of clinical signs can often be achieved with an oral dose of mg/cat every 48 hours for 1-3 weeks. This dose is then used once weekly. 10

12 DERMATOSES THAT MAY MIMICK CANINE ATOPY GOLDEN RETRIEVER ICHTHYOSIS Primary seborrheic disorder of the Golden Retriever; primary cornification and/or lipid defect? Affected individuals develop heavy scale (plate-like) which is primarily truncal in distribution but can involve the head and extremities. With chronicity, the skin tends to hyperpigment and slightly thicken (especially noted over relatively hairless, intertriginous areas such as the anterior elbows, axiallae, flanks and inguinal regions. In one study of 45 cases, age of onset was < 1 year in 20 dogs, 1-2 years in 3 dogs and > 2 years in 14 dogs. The mean age of onset was 3.6 years. We have seen this disease develop in several individuals that have been 8 or 9 years of age. The problem may wax and wane in severity. Individuals may be affected as young dogs, then go in to remission, only to recur as older individuals. The problem is non pruritic. However, it is very common to see concurrent allergic disease (e.g. atopy) in affected individuals. They will be pruritic. Concurrent allergic disease will also worsen the primary seborrheic signs. Hisotpathologic examination of biopsies from affected individuals will show severe, lamellar, orthokeratotic hyperkeratosis, no epidermal hyperplasia and no dermal inflammation. Major differential diagnoses for the problem include allergic dermatitis, hypothyroidism, cheyletiellosis and cutaneous lymphoma. Diagnosis is by rule out +/- skin biopsies. Therapeutic alternatives include the following: Option 1 combination of : Antiseborrheic shampoo e.g. Keratolux (Virbac) Conditioner Humilac (Virbac); propylene glycol; used daily or every other day Omega 3 fatty acids combination of EPA and DHA beginning at mg/kg of the combination. Omega 6 fatty acids safflower oil 0.5 ml/kg/day Oral Vitamin A 800 1,000 IU / kg divided and given BID Option 2 Option 1, initiated by intense grease baths. Patient is greased down with Alpha Keri Bath oil (or cheaper generic), diluted 50:50 with water; can be used full strength. Oil is left on for about 1 hour, then thoroughly rinsed out. More intense oil therapy is used as necessary. Option 3 Douxo Seborrhea Shampoo (phtosphingosine, cationic surface-active agents, fomblin) q 3 days for 3-4 shampoos, then either Douxo Seborrhea Micro-emulsion spray (phytosphingosine, glycerin, Botswellia serrata) q 3 days (one pump in axilla, shoulder lower back sides, ventral abdomen) or Douxo Seborrhea Spot-on (Phytosphingosine, Transcutol an excipient) 1-2 times per week (dogs less than 20 kg 1 pipette over back; kg 2 pipettes over the back; > 45 kg 3 pipettes over the back). We commonly use this regimen with omega 3 and 6 fatty acids and oral Vitamin A (see above under Option 1). IDIOPATHIC LYMPHOCYTIC/PLASMACYTIC PODODERMATITIS Affected individuals have chronic histories of pododermatitis usually affecting all feet. Predominant signs include pruritus, erythema, alopecia and localized skin thickening. Sinus tracts, and serosanguinous discharges are variably present. Sterile, hemorrhagic bullae are occasionally seen. Affected individuals are prone to secondary bacterial infections, although antibiotic therapy alone fails to produce significant benefit. Histopathologic examination of affected tissues show a perivascular accumulation of predominantly lymphocytes and plasma cells, with variable numbers of macrophages and eosinophils. All other causes for pododermatitis have been ruled out. Breeds predilected include Bull terriers, English bulldogs, Pit bulls, Boxers and Mastiffs. Other breeds may also be affected. Affected individuals do respond to glucocorticoids beginning at 2 mg/kg/day prednisone/prednisolone or cyclosporine (5 mg/kg/day). Long term maintenance therapy is often necessary. 11

13 DERMATOSES THAT MAY MIMICK FELINE ATOPY IDIOPATHIC ULCERATIVE DERMATITIS OF THE SHOULDER AREA Lesions are focal, usually singular, intensely pruritic, erosive to ulcerative and most commonly located over the dorsal interscapular region. Although reactions to subcutaneous administration of vaccines or drugs in the area has been suggested as etiologies, many affected individuals do not have a history of such treatments. Lesions will resolve if protected (e.g. e-collar, bandaging). Histopathologic findings are nonspecific (extensive ulceration accompanied by exudative crusting; adjacent dermis is often only mildly inflamed neutrophils, mixed mononuclear cells). Response to antibiotics, glucocorticoids and psychoactive drugs (e.g. clomipramine) is poor. Some claim benefit from treating with topical silver sulfadiazine, although the author has not found this to be effective. More recently, dramatic responses have been noted to oral cyclosporine (beginning at 5 mg/kg/day; increase to as much as 10 mg/kg/day if necessary). HERPESVIRUS 1 ASSOCIATED DERMATITIS AND STOMATITIS Facial Dermatitis and stomatitis has been associated with Herpesvirus 1 in domestic cats. Affected cats often have histories of recurrent or persistent mild upper respiratory tract infection. There may be a history of recent stress or the administration of glucocorticoids or drugs with glucocorticid activity (i.e. Ovaban- megestrol acetate) prior to lesion development, suggesting exacerbation of a latent viral infection. Lesions are located most commonly on the dorsal and lateral muzzle and the periorbital regions but can also be found over other haired areas of the face. The planum nasale may be affected. Lesions are characterized by erosion, ulceration, erythema, swelling, and exudation of variable degrees. The lesions may be painful and variably pruritic (can be very pruritic). A concurrent stomatitis is only occasionally noted. Histologically, there is ulceration, crusting, necrosis and a mixed dermal inflammatory infiltrate including many eosinophils. Intranuclear inclusion bodies may be present in surface and adnexal epithelium but vary in number and are less likely to be found with chronic lesions. Due to the prominent eosinophilic inflammation and low numbers of inclusion bodies, the cutaneous or oral lesions may be misinterpreted as allergic dermatitis, lesions of the eosinophilic granuloma group of disorders or mosquito bite hypersensitivity. Alternative diagnostics include immunohistochemistry for feline herpesvirus or PCR (the latter being superior). Lesions usually persist and do not respond to glucocorticoids. Treatment options include L-lysine, 250 mg (1/2 tab) BID (make sure it is form without propylene glycol); response usually seen within two to four weeks or Alpha interferon, million units / m 2 SubQ three times weekly for 4-8 weeks or 3,000 IU PO q 24 hrs or imiquimod (Aldara, 3M) topically three times weekly (note that this medication may actually cause a flare of dermatitis due to its potentially irritant nature). There are anecdotal reports of efficacy associated with the combination of L- lysine and imiquimod. There are also anecdotal reports of the use of famciclovir (Famvir, Novartis; 80 mg BID for 2-3 weeks; appears to be well tolerated in cats). ). IDIOPATHIC FACIAL DERMATITIS OF PERSIAN AND HIMALAYAN CATS Age of onset is 4 months to 5 years (median 12 months). There appears to be a heritable tendency. The first abnormality noted is usually black debris which matts the hairs of the periocular, perioral and/or chin areas. Although pruritus is often not present initially, it does develop during the course of the disease and may become moderate to severe. Affected skin becomes progressively inflamed. A bilateral erythematous otitis externa with accumulation of black waxy material within the ear canals is common. Secondary Malassezia infections are common. Secondary bacterial infections are less common but remain important potential contributor to the symptomatology. 12

14 Biopsies show marked epidermal thickening, hydropic degeneration of epidermal basal cells, occasional single cell necrosis of keratinocytes and a superficial dermal infiltrate comprised of eosinophils, neutrophils, mast cells, macrophages and occasional melanophages. Sebaceous glands are enlarged. Ectoparasites and allergies must be ruled out but the visual presence of the dark waxy material in the periocular, perioral and chin areas is highly suggestive. Secondary infections must be addressed (especially Malassezia). Response to glucocorticoids is variable and often poor. The cause of the disorder is unknown although a genetic basis is possible. More recently, this disease has shown variable response to oral cyclosporine (5-10 mg/kg/day). 13

15 CANINE AND FELINE OTOLOGY Video Otoscopy: What It Can Do For You Video otoscopes allow for excellent visualization of the ear canals and tympanum of the canine and feline ear. Reasonable visualization of the tympanic cavity (middle ear) is also possible when the tympanum has been perforated. Due to the degree of magnification, structures are better visualized than with conventional otoscopy (including degrees of inflammation, nature of debris, degree of proliferation, masses, nature and integrity of tympanum). In examination room use allows the client to visualize changes within the ear. This very commonly enhances compliance with respect to therapy. It provides easy rationalization for the need to do further diagnostics and therapeutics such as foreign body removal, deep ear cleaning or biopsies. Digital pictures and movies can be captured for the record or the client. Lens fogging tends to be one of the major impediments to adequate visualization within the ear. This often has to do with temperature differentials (warm ear, cold scope). This problem can be minimized by warming the scope tip in warm water. We have constructed a small "bulb box" that the scope head sits in during the working day to keep it warm and minimize this phenomena. If fogging is encountered, the author s routine method of cleaning the otoscope tip is to wipe it with a cotton ball soaked in alcohol. Excess alcohol is dabbed from the tip of the scope prior to going in to the ear, to minimize irritation. It is possible that this clearing may have to be done several times before adequate visualization of the ear is possible. Procedures The operating channel in the video otoscope allows for fluid infusion, passage of graspers, biopsy forceps, ear currettes, catheters, myringotomy needles and lasers. The operating channel exits the scope at 12:00 o clock. This means that all instrumentation will exit the instrument from this position. This must be considered when trying to direct instrumentation at specific areas in the ear. The video otoscope head can be turned to facilitate access to various parts of the ear. A multi-channel (2 channel) adapter allows for simultaneous running of fluids while doing other manipulative work (graspers, biopsy forceps, diode laser). Foreign body removal: grass awns etc. can often be removed on a rapid, outpatient basis, with manual restraint or light sedation, with the patient in lateral recumbancy. Deep ear cleaning is made much more effective through the use of the video otoscope. Fogging and debris accumulation (impeding visualization) may be a significant problem, but is circumvented by frequent alcohol cleaning of the tip of the scope. Cleaning: Option 1: In the anesthetized patient, the infusion of saline expands the canal and improves visualization, prevents fogging and frequently is associated with loosening up and flushing out of debris. A significant amount of debris can be removed in this fashion. Cleaning Option 2: Vetpump II (Storz); other units are available offers the option of flushing and suctioning through the same catheter, utilizing a one handed button system (video otoscope held in one hand; flushing/suctioning unit held in the other). More suction is used when working more superficially in the ear to remove large amounts of debris quickly; less suction when working deeply within the ear, especially around the tympanum. The tympanum can be perforated with excessive suction. It is always better to start with lesser amounts of suction if there is a question. Cleaning Option 3: Flushing and suctioning can be done through the working channel utilizing a 16 gage, 5.5 inch Teflon catheter (Abbot Hospital Incorporated) or a 5 inch, open ended tomcat catheter attached to a 12 cc syringe (disadvantage flushing with dirty water/saline from suctioning; difficult to see). The operating channel can also be used for passage of grabbing forceps or an ear curette to facilitate rapid debris removal. 14

16 Cleaning Option 4: Home made flushing and suction apparatus for use through the video otoscope : A 16 guage, 5.5 inch teflon jugular catheter (Abbot Hospital Incorportated, North Chicago, IL 60064), a 5.5 inch, open-ended tomcat catheter or a 3F feeding or urethral tube can be attached via an extension set to a three way stopcock. For flushing purposes, a 60 cc syringe is attached to the stopcock. The hose from a suction apparatus is then attached to the remaining portal on the 3 way stopcock. One person performs the flushing and sucking at the instruction of the individual who manipulates the scope. Cleaning Option 5: The video otoscope has a working channel to which can be attached a 2 channel adapter. The use of the adapter allows for simultaneous infusion of saline (ideally warm) and use of suction or the passage of grasping forceps or the ear curettes to facilitate debris removal. The author will also pass a cut off urethral catheter down the operating channel and do directed flushing of particularly difficult to remove debris (i.e. running fluids and flushing through the urethral catheter at the same time). Biopsies; cyst and mass removal: Biopsies utilizing the biopsy forceps are best facilitated by grasping tissue and both pulling and turning the biopsy forceps at the same time. Because biopsy samples tend to be small, they should be placed in biopsy cassettes for purposes of submission to your pathologist. The author quite routinely uses a larger pair of biopsy forceps (available from Storz) through a conventional operating otoscope to remove larger amounts of tissue, then utilizes the smaller biopsy forceps or grabbers to remove remaining tissue. Intralesional glucocorticoids for proliferative otitis externa dilute triamcinolone acetonide (6 mg/ml) to 2 mg/ml. Utilizing the Storz myringotomy needle or a 6, 22 guage spinal needle, go in to the ear as deeply as possible and inject approx. 0.1 ml of steroid within the wall of the horizontal canal or at the base of any proliferative lesions. If the canal is narrowed 360 degrees, then make 3 injections around the margins, back out 1 cm and repeat the procedure; back out again 1 cm and repeat the injections until you are out of the ear. I have generally limited my total dose per dog to 6 mg of triamcinolone. Middle ear cleaning: If the tympanum is perforated, the bulla can be flushed and aspirated as outlined above. Myringotomy may be performed through the video otoscope, utilizing a 6, 22 gage spinal needle, a Storz myringotomy needle or open ended tomcat catheter or 16 gage Teflon catheter (may help to cut tip of catheter off at an angle to facilitate penetration of the tympanum). Laser it is possible to do laser mass removal (cysts, neoplasia, proliferative tissue) and to perform myringotomies through the video otoscope (CO2 or diode laser). Visualization of the Tympanic Bulla: possible through a 2.7 or 1.9 mm arthroscope; manipulative functions are usually not possible. CANINE ALLERGIC OTITIS EXTERNA Atopy and, to a lesser degree, food sensitivity are the most common primary factors noted to initiate inflammation within the ears of the dog. In many cases, patients may have several flares of allergic otitis externa prior to developing more generalized signs of allergy. The clinician may not know that allergy is the primary factor responsible for initiating the problem (i.e. primary factor not known) until more generalized signs occur. While the otitis related to atopy and food sensitivity are usually bilateral, it is possible to see predominantly unilateral disease with both atopy and food sensitivity (even without secondary infections). 15

17 The inflammation associated with allergic otitis externa appears to preferentially target the entrance to the vertical canal. While the horizontal canal of the ear may become involved, this usually follows more chronic, severe disease or the development of secondary infections. It is common to see dilatation of the pars flaccida of the tympanum in allergic individuals (a product of head shaking?; increased air pressure within the middle ear?). Malassezia pachydermatis is the most common organism associated with secondary colonization and infection in atopic and food sensitive dogs.it is important to note that dogs may develop hypersensitivies to Malassezia and its by-products, and as such, relatively few organisms may contribute significantly to inflammation and pruritus in the ear. Secondary bacterial infections are less commonly encountered in allergic ears. Staphylococcus intermedius is most commonly seen in both acute and chronic cases. Cytologically, these are seen as cocci and diplococci on Diff Quick staining. Gram negative infections (Pseudomonas, E.coli, Kleb siella etc.) are more likely to develop in chronic cases or those that have been intermittently treated with topical antibiotics. These infections are generally seen as rods on cytologic examination. Other perpetuators of otitis that are commonly encountered in allergic otitis externa include debris accumulated within the ears and proliferative changes within the ears. Debris, especially the ceruminoliths or wads of debris that may accumulate deep within the horizontal canal serve as a source of irritation, may serve as a nidus for infection, may impede hearing and may prevent medication from getting to where it needs to get. Proliferative changes (diffuse thickening of the dermis or the development of proliferative nodues) produce a nidus for secondary infections and may impede effective access of topical medications to affected tissues. In the dog, allergic otitis externa with secondary Malassezia infection commonly results in the production of large amounts of waxy debris within the ears. However, even with chronic otitis, the tympanum is usually not perforated in these ears. Routine Treatment of Acute and Infrequently Recurrent Allergic Otitis Externa 1. At home ear flushes are prescribed for ears with significant debris. Cleanser/dryers such as EpiOtic Advanced (Virbac), Douxo Micellar Ear Solution (Sogeval; phytosphingosine containing cleanser) and Malacetic Otic (DermaPet Inc.) are used most routinely in our practice. These products have variable germicidal activity against both Malassezia and bacteria. They are usually initiated 2-4 days after starting drops, to allow the ears to quiet down (flush is more irritating than drops for most dogs). Alternative cleansers for more tenacious debris: a. Cerumene; squalane; Vetoquino). Heavier oil that will often soften drier, tenacious debris. Messy (residual oil left in hair around ear). Consider flushing ear, then flushing out the Cerumene several hours later with dilute vinegar and water or a commercial cleanser/dryer (see above). b. OtiFoam (DVM), followed by OtiRinse (DVM). c. For ears with a history of sensitivity to other flushes, consider dilute vinegar and water (1:2). Owners are instructed as to the technique of ear flushing: fill the ear; massage in for 1-2 minutes, then allow the dog or cat to shake the medication out. A cotton ball can be placed in the ear once it is filled with flush to wick debris from the ear and to facilitate cleaning the medial pinna of the ear. Ear bulb syringes and flushing/suctioning devices such as Schering s Auriflush are only rarely used to clean ears at presentation. They may be used a subsequent rechecks to facilitate debris removal (once inflammatory changes have subsided significantly). They generally do not do a good job of removing debris deep within the horizontal canal. When debris is tenacious, owners can also be taught how to use an ear bulb syringe for flushing purposes. 16